Ascent to altitude by use of airborne craft was initially achieved by hot air balloon. The first passengers carried beneath the Mongolfier brothers balloon during a 1782 flight were a duck, a rooster and a sheep, as the effects of flight for a person were unknown. At least one hundred years later, the physiological effects due to unpressurized high altitude flying remained largely unknown. In 1875, a three man balloon crew first employed a supplemental oxygen source consisting of three goatskin bags connected to a centered wash bottle providing 72 percent oxygen totaling 440 liters. The balloon flight reached 28,000 feet in altitude. While attempting to conserve oxygen during the flight, the three men were overcome by a euphoric torpor induced by lack of oxygen, resulting in the deaths of two of the men. The survivor later recorded that when convinced of the need of oxygen, he was powerless to raise his arms, unable to raise the mouthpiece of the oxygen container to his lips, and though within easy reach, the oxygen which would have saved the lives of his companions went unused. An insufficiency of oxygen in the blood is defined as hypoxemia, while an insufficiency of oxygen in the body tissue is defined as hypoxia.
To address the adverse effects of in-flight oxygen deficiency, oxygen distribution systems were incorporated into aircraft. Pre-World War II pipe stem oxygen distribution systems were later replaced by pressure clearance systems at the end of the conflict. Soon after, constant flow masks were made available in general aviation. While initial commercial air transport in the United States in the 1930's did not raise a significant risk of hypoxia because of low flight altitudes, by the 1940's to 1960's, the service ceiling of commercial aircraft was at 40,000.
Each person has a different oxygen requirement and adaptation to altitude, and those requirements change on a daily, or more accurately, an hourly basis based upon fatigue, diet, hydration level, stress and other personal factors. Increases in altitude likewise increase the associated adverse effects, including changes in visual acuity, psychomotor performance and situational awareness. As altitudes increase above 10,000 feet and critically above 15,000 feet, the time of useful consciousness (TUC) decreases at 15,000 feet to 15-20 minutes. As expected, there is a difference in the physical fitness standards between commercial/military pilots and general aviation pilots and passengers.
The Federal Aviation Administration (FAA), mindful of the adverse effects to passengers and crew of aircraft operating at altitude, has developed regulations concerning the availability and use of sustenance and supplemental breathing oxygen. These regulations are divided into the following classifications: air transport, on-demand operations and general aviation. The regulations relating to general aviation are discussed herein. The term “passengers” or “occupants” as used herein may also include the pilot and crew of the aircraft. The term “subject” as used herein may refer to any person in the aircraft. The current regulations are based on rules initially established by empirical data and experience of the Civil Aviation Administration (CAA).
Requirements for general aviation supplemental oxygen is provided in 14 CFR 91.211 as cited in the Federal Register dated Aug. 23, 2001. While this regulation provides for aircraft having pressurized and unpressurized cabins, most of the single engine piston powered general aviation aircraft used under Part 91 of the regulations employ unpressurized cabins, which is the primary focus herein. 14 CFR 91.211 provides that supplemental oxygen shall be provided to a required minimum flight crew above cabin pressure altitudes of 12,500 feet, mean sea level (MSL), up to and including 14,000 feet MSL if the duration of the flight at that altitude is more than 30 minutes. Cabin pressure altitude is calculated by taking a pressure measurement inside the aircraft cabin and converting that pressure to an altitude, preferably by a device that performs this calculation automatically. At cabin pressure altitudes above 14,000 feet MSL, the required flight crew must be provided with and use supplemental oxygen. MSL altitude is the atmospheric pressure either directly measured by weather stations at sea level or empirically determined from the weather station pressure and temperature readings collected by weather stations not at sea level. At cabin pressure altitudes above 15,000 feet MSL, supplemental oxygen must be provided to each occupant of the aircraft. In other words, FAA regulations do not require providing supplemental oxygen to occupants (passenger that are not required flight crew) below 15,000 feet MSL.
It is noted that other FAA regulations under Title 14, such as Parts 121 and 135, relate to air transport and on-demand operations, which specify different, more stringent altitude requirements with respect to supplemental oxygen use for pilots. In other words, the altitudes triggering the requirements for supplemental oxygen are greater for general aviation use. For example, 14 CFR 135.89 provides that the minimum altitude is 10,000 feet MSL instead of 12,500 feet MSL for the pilot or flight crew. The time for the required crew to use supplemental oxygen is the same 30 minute duration. As a result, many pilots may be lulled into believing that the time they spend at higher altitude is of little concern and to “push the envelope,” accepting higher altitudes when filing flight plans or maximizing the operational capabilities of their turbocharged piston powered engines without the use of supplemental oxygen. This misguided thinking has often concluded tragically. Flying at altitudes as low as 5,000 feet can affect certain individuals, particularly at night. It is estimated that pilot error is the primary cause of about 74 percent of all general aviation accidents. To understand how the present invention utilizes generally accepted clinical standards for hypoxemia, which can be easily and reliably determined and applied to help prevent hypoxia, a brief summary of human oxygen physiology is provided below.
Oxygen that is inspired through the mouth or nose proceeds down the trachea and into the main bronchi, flowing out into primary and secondary bronchi and then into the alveolar air units. The space between the mouth and the alveolar units is “dead space” because there is no air exchange in these tubes. In other words, that portion of air previously inspired only reaching this dead space retains its oxygen content and may again be inspired for air exchange. Oxygen and carbon dioxide exchanged in the alveolus is dependent on the diffusion capacity, which can be affected by age and chronic disease.
Ventilation and oxygen supplied for aerobic cellular respiration, is accomplished in the alveolar units which diffuses oxygen across the pulmonary membrane into capillary beds, the diffused oxygen in the alveolar units passing through the pulmonary cells into the pulmonary venules then into the pulmonary vein. Pressurized carbon dioxide (PCO2) from the body flows from the pulmonary artery into the capillaries, then to the alveolar unit, where it similarly diffuses through the pulmonary membrane and is expired as a waste gas. The volume of air moved through the pulmonary units is known as minute ventilation with vital capacity being the total volume of the lung.
The actual air that we breathe is a combination of different gases at various pressures P. The pressure of oxygen (PO2) is 159.1 torr in dry air, 149.2 torr in moist tracheal air at 37° C., 104 torr in the alveolar gas unit, 100 torr in arterial blood and 40 torr in mixed venous blood out of a total 760 torr at standard conditions. Thus, PO2 as used herein may be defined to refer to the oxygen pressure level corresponding to ambient, tracheal or alveolar as appropriate to apply or calculate other physiologic parameters. In addition to PO2, the partial pressures of CO2 and H2O and N2 are necessary to calculate the total and partial pressures of gases acting on the pilot (FIG. 5). The term torr refers to the pressure required to support a column of mercury 1 mm high under standard conditions, that is, standard density of mercury and standard acceleration of gravity. These conditions are at 0° C. and 45° latitude with acceleration of gravity is 980.6 cm/sec2, torr is a synonym for “mm/Hg”. An important constant to remember is the partial pressure of water vapor, for the trachea will always have a PH2O of 47 torr as inspired air will be saturated with water vapor as soon as it is inspired. Therefore only 760 torr-47 torr or 713 torr of pressure is available for the sum of pressures of oxygen, carbon dioxide and nitrogen at standard conditions of 0° C. and 45° latitude. Water vapor pressures increase with temperature, for example 20° C. has PH2O of 17.5 torr while 37° C. has PH2O of 47 torr. The PO2 of moist inspired air in the trachea is actually 149 torr, which is 20.93% of 713 torr. While the trachea will always have a PH2O of 47 torr, what of the environment from which the inspired gases are drawn into the airway of the pilot of an unpressurized aircraft at 10,000 feet MSL? As the aircraft climbs, the partial pressure of O2 and the temperature will fall with increasing altitude. Although air vents of the aircraft cabin are open to the cooler outside environment at increased altitude, typically the aircraft cabin air that is inspired by the aircraft passengers is heated and maintained at an elevated temperature for passenger comfort. Concomitantly, the ground barometric pressure and temperature will change as the aircraft navigates a course. These changes alter the baseline assumptions in actual partial pressure of gases at the indicated altitudes (IA) of the aircraft. In a pressurized aircraft such as a commercial transport aircraft pressurized at 4,000-8,000 feet MSL, a constant cabin temperature and a cabin pressure can be maintained. Over the time of a cross-country flight with decreased cabin pressure, the pilot and passenger(s) will notice lower extremity edema from lower cabin pressure relative to sea level.
For purposes herein, the pilot lung alveolar gas compartment is a critical volume. During respiration pilots expire CO2 and absorb O2 gases. The quantity (CO2 ml excreted/ml O2 absorbed) is the respiratory ratio R which gives a mean estimate of PO2 and PCO2 over time. The mean alveolar O2 (PAO2) at sea level and 37° C., is defined in equation 1
                              PAO          2                =                                            FIO              2                        ⁡                          (              713              )                                -                                    PACO              2                        ⁡                          [                                                FIO                  2                                +                                                      1                    -                                          FIO                      2                                                        R                                            ]                                                          [        1        ]            where FIO2 is the fraction of inspired O2 (percent), and PACO2 is the mean alveolar CO2. Recall that the total pressure of all alveolar gases at sea level is 760 torr. Pilot lung volumes and actual cabin altitudes will be discussed in additional detail below. As the altitude increases, the FIO2 remains relatively constant at 21%, the PAO2 decreases as the barometric pressure decreases with altitude (at 18,000 feet MSL; 50% of atmospheric pressure at sea level is absent). Therefore, the partial pressures of all gases decrease with increasing altitude. As hypoxemia is defined as the lack of adequate oxygen supply in the blood, individual pilot hypoxemia can occur at an altitude where the oxygen supply for the individual pilot is inadequate for the pilot physiologic oxygen demand. The key factor is not a specific aircraft altitude MSL but rather the oxygen demand of the pilot. The diffusion capacity of the gases varies with the individual, dependent on the current status of the health of the pilot's lung alveolus. The oxygen diffuses from the alveolus to the venue capillary into the blood serum and then is absorbed by the red cell and stored there for transport in the body.
The components of the oxygen transport system are comprised of cardiac output of the heart (CO), the hemoglobin concentration of the blood (Hb), oxygen red cell saturation of the red blood cells (SAO2) for arterial circulation, (SVO2) for venous circulation, and the oxygen consumption of the body (VO2). Oxygen saturation is defined as the percentage of oxygen bound hemoglobin to the total amount of hemoglobin available. Oxygen saturation in the blood may be measured by a co-oximeter in the pulmonary laboratory.
Invasive medical oxygen moniters or oximeters, such as those originally manufactured by Oximetrix Inc., of Mountain View, Calif., may include a catheter, an optical module and a digital processor. The catheter, such as a pulmonary artery catheter typically includes a balloon on a distal tip for flow-directed placement, and a proximal lumen, which is a thermistor similar to a standard pulmonary artery thermodilution catheter, and two optical fibers. One fiber transmits light from the optical module to the distal tip of the catheter while the second fiber returns the reflected light from the distal tip back to the optical module. The Oximetrix optical module contains three light emitting diodes (LED's) that illuminate, via one optical fiber, the blood flowing past the catheter tip. Light reflected from the blood is returned through the second fiber and directed into a solid state photodiode detector within the optical module. The module converts the light intensity levels into electrical signals for transmission to the processor. The digital processor computes percent of oxygen saturation values based on the electrical signals transmitted and received from the optical module. These values are continuously displayed in numerical form by LED and are recorded by the processor's built-in strip recorder. Later models have LED display only but functionally are the same unit.
Oximeters have been used under clinical conditions, especially for monitoring oxygen saturation levels of critically ill patients. However, catheters, such as Opticath® catheters which are used with Oximetrix oxygen monitors, are invasive as the catheter must be inserted inside the pulmonary artery. Alternately, oxygen saturation may also be measured transcutaneously using infrared light in pulse oximetry units. Pulse oximeters similarly employ an LED and photosensor placed on opposite sides of arterioles located in a subject's tissue that can be transilluminated. In other words, pulse oximeters may be positioned over a narrow portion of a subject's anatomy, such as a finger or ear lobe. Typically, the pulse oximeter “clips” over opposed sides of the end of an appendage, such as an index finger. Pulse oximeters have many advantages over Opticath® catheters. They are noninvasive, as the subject's skin is not pierced, require no calibration, provide nearly instantaneous readings, rarely provide false negative information, require no routine maintenance, and are relatively inexpensive to purchase. These units are accurate in normal physiologic states, although in clinical situations of hypoprofusion and hypothermia the transcutaneous oxygen saturation measurements are inaccurate. Oxygen saturation measured in a pulmonary artery by either direct blood measurement (blood gas studies) or fiber-optic pulmonary artery catheter (co-oximetry) or pulse oximetry is generally accurate within 2% of the actual value.
Co-oximetry and pulse oximetry provide measurements of hemoglobin saturation. Molecular oxygen is carried within the hemoglobin molecule to tissues in the body, the oxygen carrying capacity possibly varying over time in response to changing health and/or environmental conditions. Normal hemoglobin carries 98% of the oxygen within the hemoglobin molecule with approximately 2% of the oxygen in the blood serum. This, however, can change significantly in diseases such as sickle-cell anemia (HbSS>50%) in which there is abnormal sickling of the hemoglobin molecule and decrease in oxygen carrying capability. This can be aggravated in periods of hypotension and dehydration even in sickle cell trait (HbSS<50%). Oxygen transport (O2T) occurs best at hemoglobin values of 40-43%. At hematocrit values greater than 50%, the result is increased viscosity and sluggishness of the blood, whereas hematocrit values less than 40% have the result of decreased hemoglobin and therefore less molecular oxygen saturation, a result of anemia. Oxygen content relates to the ability of the subject to adjust to physiologic stress.
The driving force in the oxygen transport system is the heart and resultant cardiac output (CO). The cardiac output is typically about 5.0 liters per minute, with maximums up to about 15.0 liters per minute during exercise. However, cardiac output can drastically fall to about 1.0 or 2.0 liters per minute in states of heart failure. In normal hemostasis with normal hemoglobin cardiac output, and adequate oxygenation there should be sufficient oxygen content in the blood and this content will be transported to peripheral tissues for consumption. Provided below are some equations relating to the oxygen transport system.
Equations of the Oxygen Transport System1.Oxygen Saturation (%)       SO    2    =                    HBO        2                    Hb        +                  HBO          2                      ×    100   Arterial (SAO2) 91%–97%Venous (SVO2) 60%–75%2.Oxygen Content (CO2) (mL O2/100 mL blood = vol %) arterial(2% O2, dissolve) + (98%/O2 Hb saturated)ArterialCAO2 = (PO2 × 0.0031) + (Hb × 1.38 × SAO2)CAO2 = (100 torr × 0.0031) + (15 g × 1.38 × .97)CAO2 = .3 + 20.1CAO2 = 20.4 vol. %VenousCVO2 = (PVO2 × 0.0031) + (Hb × 1.38 × SVO2)CVO2 = (40 torr × 0.0031) + (15 g × 1.38 × .75)CVO2 = .12 + 15.52CVO2 = 15.64 vol. %3.Oxygen Transport (O2T) (mL O2 /min)Arterial: O2TA = CO × CAO2 × 10Venous: O2 TV = CVO2 × 104.Oxygen Consumption (VO2) (mL O2/min)VO2 = CO × Hb × 1.38 (SAO2 − SVO2) × 10VO2 = 5 L/min × 15 g × 1.38 (.97 − .75) × 10VO2 = 228 mL/min5.Cardiac Output (L/min)   CO  =            VO      2                      CAO        2            -              CVO        2            